Paramecium aurelia and its mutants are used as a model system for excitable membranes. The protozoan exhibits a voltage-dependent increase in calcium conductance, and its pawn mutant fails to show this change in calcium conductance. Hence, an excitable membrane has genetically been altered to an inexcitable membrane. This alteration manifests itself in a behavioral change; i.e. the inability to swim backward. Normal membranes, after depolarization, apparently allow external calcium to enter and raise the calcium concentration around the ciliary locomotory apparatus to a threshold which causes a change of the effective stroke of the cilia. Other laboratories are emphasizing genetic and electrophysiological approaches to understanding this system. This project emphasizes the biochemical and structural aspects. Detailed lipid and protein analysis, ultrastructural observations of cells treated by a variety of methods, and ionophore effects on behavior are studies planned for this project.